Antagonism of the antinociceptive effect of nitrous oxide by inhibition of enzyme activity or expression of neuronal nitric oxide synthase in the mouse brain and spinal cord

Jessica Lack Cope; Eunhee Chung; Yusuke Ohgami; Raymond M Quock

doi:10.1016/j.ejphar.2009.09.059

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Antagonism of the antinociceptive effect of nitrous oxide by inhibition of enzyme activity or expression of neuronal nitric oxide synthase in the mouse brain and spinal cord

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Antagonism of the antinociceptive effect of nitrous oxide by inhibition of enzyme activity or expression of neuronal nitric oxide synthase in the mouse brain and spinal cord

Jessica Lack Cope, Eunhee Chung, Yusuke Ohgami and Raymond M Quock

European journal of pharmacology, Vol.626(2), pp.234-238

2010

DOI: https://doi.org/10.1016/j.ejphar.2009.09.059

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https://hdl.handle.net/2376/113376

PMCID: PMC2790018

PMID: 19818753

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Abstract

Antinociception

Antisense

Nitrous oxide

NOS-inhibitor

Nitric oxide

Transgenic mice

Previous studies have implicated nitric oxide (NO) in the antinociceptive response to the anesthetic gas nitrous oxide (N 2O). The present study was conducted to confirm this NO involvement using pharmacological and gene knockdown and knockout strategies to inhibit the supraspinal and spinal production of NO. Antinociceptive responsiveness to 70% N 2O was assessed using the acetic acid (0.6%) abdominal constriction test in NIH Swiss mice following intracerebroventricular (i.c.v.) or intrathecal (i.t.) pretreatment with the NOS-inhibitor l-N G-nitro arginine methyl ester (L-NAME) or an antisense oligodeoxynucleotide (AS-ODN) directed against neuronal NOS (nNOS). Experiments were also conducted in mice homozygous for a defective nNOS gene (nNOS −/−). Mice that were pretreated i.c.v. or i.t. with L-NAME (1.0 µg) both exhibited 80–90% reduction in the magnitude of the N 2O-induced antinociceptive response. Mice that were pretreated i.c.v. or i.t. with nNOS AS-ODN (3 × 25 µg) exhibited a 60–80% antagonism of the antinociceptive response. Compared to wild-type mice, nNOS knockout mice showed a 60% reduction in N 2O-induced antinociception. These findings consistently demonstrate that transient or developmental suppression of nNOS expression significantly reduces antinociceptive responsiveness to N 2O. NO of both supraspinal and spinal origin, therefore, plays an important role in the antinociceptive response to N 2O.

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Title: Antagonism of the antinociceptive effect of nitrous oxide by inhibition of enzyme activity or expression of neuronal nitric oxide synthase in the mouse brain and spinal cord
Creators: Jessica Lack Cope - Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, Washington 99164-6534, USA
Eunhee Chung - Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, Washington 99164-6534, USA
Yusuke Ohgami - Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, Washington 99164-6534, USA
Raymond M Quock - Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, Washington 99164-6534, USA
Publication Details: European journal of pharmacology, Vol.626(2), pp.234-238
Academic Unit: Psychology, Department of
Publisher: Elsevier B.V
Identifiers: 99900547654501842
Language: English
Resource Type: Journal article